22,380 research outputs found

    Nerve damage surveillance

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    Inferior Alveolar Nerve Injury Caused by Coronectomy or Conventional Method in Third Molar Extractions

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    To compare the frequency of injury to the inferior alveolar nerve as a result of coronectomy and removal of mandibular third molars having nerve approximation.Methods: In this comparative study 110 patients with inferior alveolar nerve approximation were selected and randomly allocated into Group-A and Group-B. Group-A patients underwent coronectomy and Group-B patients underwent traditional removal. Inferior alveolar nerve damage was assessed one week post operatively, then further assessed after 01, 03 and 06 months.Results: Out of total 110 patients included in the study, 9 (8.2%) patients were having nerve damage. In traditional removal group, 9 (16.4%) patients were found to have nerve damage. Seven patients with nerve injury recovered within 06 months whereas 2 patients had permanent nerve damage. In coronectomy group none of the patients had nerve damage.Conclusion: Coronectomy is an effective procedure in significantly reducing the incidence of inferior alveolar nerve injury when compared with traditional removal of wisdom teeth

    Analysis of Antibody and Cytokine Markers for Leprosy Nerve Damage and Reactions in the INFIR Cohort in India

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    Leprosy is one of the oldest known diseases. In spite of the established fact that it is least infectious and a completely curable disease, the social stigma associated with it still lingers in many countries and remains a major obstacle to self reporting and early treatment. The nerve damage that occurs in leprosy is the most serious aspect of this disease as nerve damage leads to progressive impairment and disability. It is important to identify markers of nerve damage so that preventive measures can be taken. This prospective cohort study was designed to look at the potential association of some serological markers with reactions and nerve function impairment. Three hundred and three newly diagnosed patients from north India were recruited for this study. The study attempts to reflect a model of nerve damage initiated by mycobacterial antigens and maintained by ongoing inflammation through cytokines such as Tumour Necrosis Factor alpha and perhaps extended by antibodies against nerve components

    Contemporary Perspectives in Pathophysiology of Facial Nerve Damage in Oto-Neurological and Skull Base Surgical Procedures: A Narrative Review

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    During the last decades, neuro-otological surgery has progressively reduced functional morbidity, including facial nerve damage. However, the occurrence of this sequela may significantly impact on patients’ quality of life. The aim of this narrative review is to provide an update on the patho-physiological and clinical issues related to facial nerve damage in oto-neurological and skull base surgery, in the light of a comprehensive therapeutic and rehabilitative approach to iatrogenic disfunctions. The narrative review is based on a search in the PubMed, Scopus, andWeb of Science databases. In this surgical setting, the onset of intraoperative facial nerve damage is related to various aspects, mainly concerning the anatomical relationship between tumor and nerve, the trajectory of the surgical corridor, and the boundaries of the resection margins. Mechanisms related to stretching, compression, devascularization, and heating may play a role in determining intraoperative facial nerve damage and provide the patho-physiological basis for possible nerve regeneration disorders. Most of the studies included in this review, dealing with the pathophysiology of surgical facial nerve injury, were preclinical. Future research should focus on the association between intraoperative trauma mechanisms and their clinical correlates in surgical practice. Further investigations should also be conducted to collect and record intraoperative data on nerve damage mechanisms, as well as the reports from neuro-monitoring systems

    Demyelination in Leprosy

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    Leprosy is a chronic infectious disease caused by Mycobacterium leprae that has a predilection for peripheral nerves, especially Schwann cells (SCs). Leprosy medications may only eradicate the bacteria without preventing or recovering peripheral nerve damage. Early nerve damage detection is necessary. The expression of Krox-20 in Schwann cells will be examined immunohistochemically, and the level of neuron growth factor (NGF), neuregulin 1 (NRG1), protein 0 (P0), and peripheral myelin protein 22 (PMP22) will be examined in the blood plasmas. A significant decrease was noticed in Krox-20 and NGF, NRG1, P0, and PMP22 level (p < 0.05) in disability degree 1 compared to degree 0. Studies proved that markers have shown promising results; Krox-20, NGF, NRG1, P0, and PMP22 could be useful diagnostic tools for early peripheral nerve damage detection in leprosy

    Altered expression of the voltage-gated calcium channel subunit α2δ-1: a comparison between two experimental models of epilepsy and a sensory nerve ligation model of neuropathic pain.

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    The auxiliary α2δ-1 subunit of voltage-gated calcium channels is up-regulated in dorsal root ganglion neurons following peripheral somatosensory nerve damage, in several animal models of neuropathic pain. The α2δ-1 protein has a mainly presynaptic localization, where it is associated with the calcium channels involved in neurotransmitter release. Relevant to the present study, α2δ-1 has been shown to be the therapeutic target of the gabapentinoid drugs in their alleviation of neuropathic pain. These drugs are also used in the treatment of certain epilepsies. In this study we therefore examined whether the level or distribution of α2δ-1 was altered in the hippocampus following experimental induction of epileptic seizures in rats, using both the kainic acid model of human temporal lobe epilepsy, in which status epilepticus is induced, and the tetanus toxin model in which status epilepticus is not involved. The main finding of this study is that we did not identify somatic overexpression of α2δ-1 in hippocampal neurons in either of the epilepsy models, unlike the upregulation of α2δ-1 that occurs following peripheral nerve damage to both somatosensory and motor neurons. However, we did observe local reorganisation of α2δ-1 immunostaining in the hippocampus only in the kainic acid model, where it was associated with areas of neuronal cell loss, as indicated by absence of NeuN immunostaining, dendritic loss, as identified by areas where microtubule-associated protein-2 immunostaining was missing, and reactive gliosis, determined by regions of strong OX42 staining

    Käden postoperatiivinen kuntoutus hermovaurion jälkeen

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    Hermovaurion postoperatiivinen kuntoutus on moninainen prosessi. Jotta fysioterapeutti pystyy suun-nittelemaan kuntoutusprosessin sisällön harjoitteineen ja valitsemaan oikeat terapiamuodot, on hänen ymmärrettävä käden anatomia ja toiminta sekä vaurion vaikutukset siihen. Opinnäytetyön tarkoitus on selvittää, mitkä tekijät vaikuttavat käden hermovaurion postoperatiiviseen kuntoutukseen ja vaurion paranemisennusteeseen sekä millainen on kuntoutuspolku kaikkine mahdolli-suuksineen hermovaurioleikkauksen jälkeen. Opinnäytetyömme toteutettiin kirjallisuuskatsauksena, jossa selvitettiin hermokudoksen anatomiaa sekä käden alueen hermotusta. Lisäksi fysioterapian kannalta koottiin olennaista tietoa hermovaurioiden syn-tymekanismeista, kirurgisen hoidon pääpiirteistä, hermon uusiutumiseen liittyvistä tekijöistä sekä kun-toutuksesta. Teoriaosuuteen koottiin tämän hetken näyttöön perustuvaa tietoa suomen- ja englanninkieli-siä artikkeleita, kirjallisuutta sekä tutkimuksia. Teorian pohjalta tehtiin syventäviä asiantuntijahaastatte-luja fysioterapeuteille ja toimintaterapeuteille. Tällöin kirjallisuuskatsauksessa löydettyä tietoa pystyttiin täydentämään ja myös käytännön näkökulma saatiin opinnäytetyöhön myös esille. Opinnäytetyö on tehty Mikkelin ammattikorkeakoulun Savonlinnan kampuksen palveluyksikkö Elixiirin käyttöön. Opinnäytetyö toimii ensisijaisesti opetusmateriaalina fysioterapiaopiskelijoille, mutta uskomme, että siitä hyötyvät myös fysio- ja toimintaterapeutit, jotka työskentelevät hermovaurion postoperatiivisen kuntoutuksen parissa.The postoperative rehabilitation of nerve damage is a multifold process. In order to plan a rehabilitation program with exercises and choose the right therapy, the physiotherapist must understand the anatomy and function of the hand and how it is influenced by nerve damage. The purpose of this thesis is to find out which factors have an influence to the postoperative rehabilitation of the hand after nerve damage and to the prognosis of recovery, as well as the possibilities of designing a rehabilitation programme for a patient after a nerve damage operation. The thesis was executed as a literature review. Nerve tissue anatomy and nerves of the arm were examined. Also the main points of physiotherapy, the leading causes of nerve damage, the main characteristic of surgical treatment, factors of nerve regeneration, and nerve rehabilitation programs were researched. The literature review covers evidence-based, Finnish and English language articles, literature and researches. The theoretic background formed the basis for conducting interviews with experts such as physiotherapists and occupational therapists. This allowed a deeper understanding of the topic while giving the thesis a practical perspective as well. The thesis is made to be used in Elixiiri, the Center of Welfare Services at the Savonniemi Campus of Mikkeli University of Applied Sciences. The primary purpose is to offer study material for physiotherapy students but it can be useful to physiotherapists and occupational therapists who work with postoperative rehabilitation clients after nerve damage in the hand

    Prevention of neurological injuries during mandibular third molar surgery: technical notes

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    Surgery to the mandibular third molar is common, and injuries to the inferior alveolar nerve and the lingual nerve are well-recognized complications of this procedure. The aim of these technical notes is to describe operative measures for reducing neurological complications during mandibular third molar surgery. The following procedure should be used to prevent damage to the inferior alveolar nerve: a well-designed mucoperiosteal flap, to obtain appropriate access to the surgical area; a conservative ostectomy on the distal and distal-lingual side; tooth sectioning, to facilitate its removal by decreasing the retention zones; tooth dislocation in the path of withdrawal imposed by the curvature of the root apex; and careful socket debridement, when the roots of the extracted tooth are in intimate contact with the mandibular canal. To prevent injury to the lingual nerve, it is important (I) to assess the integrity of the mandibular inner cortex and exclude the presence of fenestration, which could cause the dislocation of the tooth or its fragment into the sublingual or submandibular space; (II) to avoid inappropriate or excessive dislocation proceedings, in order to prevent lingual cortex fracture; (III) to perform horizontal mesial-distal crown sectioning of the lingually inclined tooth; (IV) to protect the lingual flap with a retractor showing the cortical ridge; and (V) to pass the suture not too apically and from the inner side in a buccal-lingual direction in the retromolar are

    Nerve damage induced skeletal muscle atrophy is associated with increased accumulation of intramuscular glucose and polyol pathway intermediates

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    Perturbations in skeletal muscle metabolism have been reported for a variety of neuromuscular diseases. However, the role of metabolism after constriction injury to a nerve and the associated muscle atrophy is unclear. We have analyzed rat tibialis anterior (TA) four weeks after unilateral constriction injury to the sciatic nerve (DMG) and in the contralateral control leg (CTRL) (n = 7) to investigate changes of the metabolome, immunohistochemistry and protein levels. Untargeted metabolomics identified 79 polar metabolites, 27 of which were significantly altered in DMG compared to CTRL. Glucose concentrations were increased 2.6-fold in DMG, while glucose 6-phosphate (G6-P) was unchanged. Intermediates of the polyol pathway were increased in DMG, particularly fructose (1.7-fold). GLUT4 localization was scattered as opposed to clearly at the sarcolemma. Despite the altered localization, we found GLUT4 protein levels to be increased 7.8-fold while GLUT1 was decreased 1.7-fold in nerve damaged TA. PFK1 and GS levels were both decreased 2.1-fold, indicating an inability of glycolysis and glycogen synthesis to process glucose at sufficient rates. In conclusion, chronic nerve constriction causes increased GLUT4 levels in conjunction with decreased glycolytic activity and glycogen storage in skeletal muscle, resulting in accumulation of intramuscular glucose and polyol pathway intermediates
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